Enhanced sodium-calcium exchange in the infarcted heart: effects on sarcoplasmic reticulum content and cellular contractility.

Arrhythmias and contractile dysfunction both contribute to the high morbidity and mortality in patients with congestive heart failure. Contractile dysfunction is generally believed to reflect a decrease in the amplitude of intracellular Ca2+ transients, whereas tachyarrythmias are often initiated in the setting of cellular Ca2+ overload. In a rabbit model of left ventricular dysfunction due to myocardial infarction, we found evidence that myocyte sarcoplasmic reticulum Ca2+ content may be normal or even increased at slow stimulation rates. This may occur because prolonged action potential duration promotes Ca2+ influx via the Na+/Ca2+ exchanger. Despite preserved SR Ca2+ content, intracellular Ca2+ transients and contractions may be reduced in amplitude because of impaired synchronization of Ca2+ release events throughout the myocyte.